Since progesterone secretion by the corpus luteum is essential for normal pregnancy, interruption of this secretion would be a logical method of contraception. However, we do not understand completely the complex endocrine and biochemical mechanisms involved in regulation of progesterone secretion. Therefore, experiments are proposed which would provide new information regarding the effects of selected hormones on the number of LH receptors, the synthesis and degradation of LH receptors and the effects of LH on the quantity and the activity of the major steroidogenic enzymes in the ovine corpus luteum. Numbers of LH receptors will be quantified during different reproductive states using oLH-125I in combination with Scatchard analyses and radioimmunoassay of endogenous LH bound to receptor. To study the chronic effects of LH, PGF2 alpha and prolactin on the number of LH receptors these hormones will be infused or injected and/or specific antibodies will be used to neutralize the endogenous hormones. In vitro studies will be performed with cultured luteal cells to ascertain if LH, prolactin and PGF2 alpha influence the synthesis and degradation of LH receptors. These studies are important since the number of receptors for LH in luteal tissue is the initial point at which LH regulates stimulation of secretion of progesterone. A second series of experiments will be conducted to ascertain whether LH, prolactin and PGF2 alpha exert a chronic influence on the quantity and/or activity of the four major steroidogenic enzyme complexes within the corpus luteum. These enzymes will be quantified in kinetically valid enzyme assays while the activity of these enzymes in intact cells will be studied by monitoring the conversion of radioactive steroid substrates to product. The acute effects of LH and PGF2 alpha on the activity of the steroidogenic enzymes will also be evaluated in vitro. If the activity of these enzymes is modified without changes in the quantity of enzyme then experiments will be conducted to evaluate the role of transport proteins which may increase availability of substrate or relieve end-product inhibition and thus modulate the activity of the steroidogenic enzymes.